Blog

Pregnant women have heard it time and time again: What you eat during those nine months can have long-term effects on your child’s health. Heck, one study even that when pregnant women eat a diverse diet, the resulting babies are less picky in the foods they choose. So what about mom’s eating habits before she even knows she’s pregnant? Nutritional deficiencies right at the time of conception can alter a baby’s genes permanently, scientists at the London School of Hygiene and Tropical Medicine Tuesday. The study, published in Nature Communications, is the first to show that an environmental factor during the first few days of development can change DNA long term. The researchers didn’t look at how these genetic changes affect overall fetal development or the baby’s health later in life. And they analyzed only six genes. But there’s growing from other studies that similar types of genetic changes may help determine a child’s risk for some diseases, including diabetes, mental disorders and autism. “Can diet affect other genes? What’s the biological impact of those [DNA] modifications? At the moment we don’t know the answer to those questions,” says nutritionist , who contributed to the study. “But subsequent research we have — and haven’t [yet] published — says it does matter.” Now we’re not talking about altering the DNA code itself — you know, the building blocks of genes, the ? Rather, Prentice says the dietary effects he and his team have found seem to be changing whether genes are turned on or off in that earliest stage of embryonic development. This on-and-off switch is controlled by decorating the DNA with a special tag, called . How much the six genes got tagged in the developing embryo depended on the levels of a few micronutrients in the mom’s blood at the time of conception, Prentice and his team found. The team examined several B vitamins and nutrients associated with them. They couldn’t pinpoint exactly which ones were most important. But in general, when several of these nutrients, including vitamin B2, were at lower levels in mom’s blood, the six genes had less methylation. “The vitamin levels [in all the women] weren’t way out of the normal range either,” Prentice says. “If you took the blood to your doctor, he would say they were normal.” The team also found a link between the DNA methylation and mom’s body mass index at the time of conception. The heavier the mother, the less methylation. And again, none of the moms were obese. “There were no overweight women in this group,” Prentice says. “Even then, we found a strong link between the mother’s BMI and methylation patterns.” For years, scientists have observed a similar phenomenon in mice: Diet and weight, at the time of conception, alter a baby’s DNA methylation. To check for the effect in people, Prentice and his team turned to women in . Families there rely on their gardens for most of their food, he says, “so the weather patterns completely change the foods eaten throughout the year.” In the rainy season, residents get fewer calories but more nutrient-rich vegetables. In the dry season, they have more calories but dishes are less vitamin-packed. “I think the study is great,” says Duke University’s , who wasn’t involved in the work. “We’ve...

Reprinted from NATIONAL GEOGRAPHIC Rampant disagreement over what constitutes Lyme disease—in particular, who may have contracted it and how, and how long it lasts—has spawned the larger question of how best to treat it. A new study pointing to the possibility of sexual transmission of the pathogen adds fuel to the fire. Amid the uncertainty, a patient-led lobby (the counterculture, as someone has called it) that includes doctors as well as Lyme sufferers advocates a broader definition of the disease, both for treatment and insurance purposes. But the medical establishment asserts that too liberal a definition—and what are seen as renegade practitioners—has led to irresponsible and potentially dangerous treatment of unrelated maladies misidentified as Lyme. It’s also unknown how many people have died because of Lyme. A 2011 study found that of the 114 deaths reported over a five-year period listing Lyme as a partial or direct cause, only one was consistent with clinical manifestations described by the International Classification of Diseases. In December 2013, the Centers for Disease Control and Prevention (CDC) confirmed that Lyme carditis—a condition in which the Lyme bacterium infects the heart—caused three deaths over the past two years. Between 1985 and 2008, only four other fatal cases were confirmed. While the course of the illness varies greatly from person to person, initial manifestations can include a unique skin lesion known as erythema chronicum migrans, headaches, musculoskeletal pain, coughing, sore throat, conjunctivitis, and minor neurological impairment. If the diagnosis is confirmed early enough, Lyme is treated almost exclusively with short-term antibiotics, often penicillin, which are almost 100 percent effective. But if Lyme goes untreated, symptoms can progress. (Watch related video: “The Deer Tick”) In Lyme’s second stage, typically between one and several months after the initial infection, neurological abnormalities can arise, such as meningitis, encephalitis, and cranial neuritis, which can manifest as facial palsy. Some patients develop cardiac problems. In the third stage, which can take several months to years to show up, many patients develop chronic arthritis as well as an increase in neurological and cardiac symptoms, the severity of which can ebb and flow. Voices in the counterculture argue that Lyme’s symptoms are more intense and longer lasting than the medical establishment acknowledges. They say that symptoms of chronic Lyme disease are responsible for related deaths, including suicides from depression about the disease or from the trauma of persistent debilitating symptoms such as arthritis, heart problems, and cognitive impairment. New Developments And now, further complicating the picture, a study published this January contends that Lyme disease may be sexually transmitted. It shows that the Lyme pathogen, Borrelia burgdorferi (Bb), has been found in both male and female sexual secretions, raising the question of whether people are at risk through intimate contact. Bb is one of only six known spirochete bacteria, named for their coiled spiral shape. (One of the six is the bacterium responsible for syphilis.) PHOTOGRAPH BY SCIENCE PICTURE CO., CORBIS Borrelia burgdorferi is the bacterial agent of Lyme disease. The primary vector for Bb is the deer tick—Ixodes scapularis—although other kinds of ticks have been known to transmit it, and other insects, including some mosquitoes, carry the pathogen. A study of Bb last year revealed that it’s the first known organism that doesn’t need iron to survive. This allows it...

It’s not difficult to understand the appeal of Wi-Fi. This revolutionary technology, which has been commercially available since 1999, eliminates cabling and wiring for computers, reduces cellular usage charges and allows us to connect to the Internet from anywhere with a signal. Despite these benefits, however, studies continue to show that the radiation generated by wireless routers is negatively affecting our health. In fact, the British activist website Stop Smart Meters recently published a list of 34 scientific studies demonstrating the adverse biological effects of Wi-Fi exposure, including studies linking it to headaches, reduced sperm count and oxidative stress. The latest research into the dangers of Wi-Fi, though, comes from a surprisingly humble source: Five ninth grade female students from Denmark, whose science experiment revealed that wireless radiation is equally as devastating to plants. Undeniable results The experiment began when the five students realized that they had difficulty concentrating in school if they slept near their mobile phones the previous night. Intrigued by this phenomenon, the students endeavored to study the effects of cellphone radiation on humans. Unfortunately, their school prevented them from pursuing this experiment due to a lack of resources, so the students decided to test the effects of Wi-Fi radiation (comparable in strength to cellphone radiation) on a plant instead. The girls placed six trays of Lepidium sativum seeds (a garden cress grown commercially throughout Europe) in a room without radiation, and an equal amount in a room next to two Wi-Fi routers. Over a 12-day period, they observed, measured, weighed and photographed the results. Even before the 12th day arrived, however, the end results were obvious: The cress seeds placed near the routers either hadn’t grown or were completely dead, while the seeds placed in the radiation-free room had blossomed into healthy plants. The experiment earned the five students top honors in a regional science competition. Moreover, according to a teacher at their school, Kim Horsevad, a professor of neuroscience at the Karolinska Institute in Sweden was so impressed with the experiment that he is interested in repeating it in a controlled scientific environment. READ...

Skin: It is your body’s largest organ, and groundbreaking new research out of Denmark has found that the proper function of your other vital organs is dependent upon its integrity. A collaborative research project out of the University of Southern Denmark (USD) recently discovered that human skin directly communicates and interacts with the rest of the body, meaning that, when it is not in good health, there is a good chance that the same is true about other vital organs. Professor Susanne Mandrup and her team stumbled upon this finding while researching something else, which she says came as quite a shock. While working with Nils Faergeman’s research group at USD’s Department of Biochemistry and Molecular Biology, Mandrup and her team observed that human skin literally “talks” to other vital organs, including the liver, which is responsible for filtering out toxins and processing carbohydrates and fats. According to Science Daily, the team had been conducting research on so-called “knock-out” mice, or mice that lack a special fat-binding protein known as acyl-CoA-binding protein, when they made the discovery. Some of the mice had strange, greasy fur and were having difficulties being weaned from their mothers, prompting researchers to take a closer look. Since these same mice were having difficulties processing fat through their livers, instead accumulating it over time, the team initially assumed that this probably had something to do with their missing liver genes. But after taking a closer look and conducting a series of experiments, it became clear that there was some other factor involved in this metabolic abnormality. “At first we thought that the fat accumulation in the liver was linked with the fact that the gene was missing in the liver of the knock-out mice,” stated Ditte Neess, one of the researchers. “But this was ruled out by a series of studies, and we had to find another explanation.” Unhealthy skin can lead to unhealthy organs, reveals study When they decided to take a second look at the mice, a combination of greasy fur and what appeared to be “leaky” skin led the team to some new conclusions. Since the leaky skin mice appeared to be losing more water than the other mice, making them colder, researchers hypothesized that this, and not the missing gene, was somehow responsible for a corresponding fat accumulation in the mice’s livers. “When they lose water, they also lose heat,” added Neess. “We therefore asked ourselves whether this water and heat loss could be the reason why the mice accumulated fat in the liver and became weak when weaned from their mother.” As it turns out, this hypothesis was correct. The knock-out mice with the skin and fur problems were more prone to fat accumulation in their livers, and this was the result of their unhealthy skin. After applying a petroleum-based jelly to the coats of the mice in question, and later liquid latex, both of which stopped the heat loss in the mice, their fat accumulation issues also stopped. “We have showed that the skin affects the metabolism in the liver, and that is quite a surprise,” stated the team. “We believe that the leaking of water from the skin makes the mice feel cold, and that this leads to breaking down of fat in their adipose (fat) tissue. The...

Research has shown that some common bacteria are consistently detected in the central nervous system of Alzheimer’s patients.1 Doctors from the International Alzheimer Research Center in Switzerland published a study indicating a high probability of a causal relationship, not just an association, between spirochete infections and Alzheimer’s disease. What they discovered was pretty amazing. They found spirochetes in about 90% of Alzheimer’s patients, while the bacteria were virtually absent in healthy age-matched controls.1 Could Alzheimer’s disease be caused by this infection? Let’s explore. Spirochetes Form Brain Plaques Much insight about what could happen in the brain during this process comes from studies on a spirochete, Borrelia burgdorferi, which is the cause of Lyme disease. Spirochete infection begins with the bacteria entering the brain. Once within the brain tissue, they cause disease by forming plaques or masses along the cerebral cortex — the surface of the brain. Agglutination in the center of the plaque results in a homogeneous central core, which attracts brain macrophages, called microglial cells. The macrophages are responsible for recognizing foreign invaders, engulfing them and presenting them to bacteria fighting immune cells. The macrophages become trapped within the core of the spirochete plaque. Once trapped, they are vulnerable to attack by the spirochetes. This results in their dysfunction and diminished capacity for fighting the infection. The infection spreads and begins to damage and kill brain cells.2 Damaged brain cells produce the characteristic amyloid-beta protein seen in Alzheimer’s patients. Now here’s where it gets really interesting… Amyloid-beta Protein has Antibacterial Properties Scientists have discovered that amyloid-beta protein has anti-bacterial properties, indicating that its production may be an adaptive response to infectious organisms, like invading spirochetes.3,4 The whole process may work something like this: Spirochetes invade and infect the brain. The brain’s normal defenses become dysfunctional as the macrophages (microglia) become trapped and then attacked within the core of the spirochete plaque. With immune dysfunction setting in, the spirochete infection intensifies involving more and more brain cells. Damaged brain cells produce amyloid-beta protein as an adaptive response to the infection. Amyloid-beta deposits grow and begin to affect brain cell connections and communication highways. With damaged connections and communication highways, dementia symptoms begin and gradually worsen. Early Intervention with Antibacterials These findings have led some researchers to hypothesize that “…early intervention against infection may delay or even prevent the future development of Alzheimer’s disease.”3 Early intervention might include preventative antibacterial remedies in people at high risk of developing Alzheimer’s — a person with a strong family history or the presence of the Apo-E4 allele (a lipoprotein used for fat and cholesterol transport).5 Antibacterial herbs and other remedies could also be used as part of the early treatment regimen in patients diagnosed with Alzheimer’s disease. Reversing Macrophage Dysfunction with Curcumin Here’s something amazing: Curcumin helps enhance the engulfing properties of brain macrophages — the same macrophages that are damaged and dysfunctional by the spirochetes. As it turns out, curcumin can bind to amyloid-beta plaques, allowing the brain macrophages to “latch on” and engulf the plaques. The clearing of the plaques can help resolve the infection and reestablish normal brain cell connections and communication highways.6 Could antibacterial remedies and curcumin make up an early Alzheimer’s prevention and treatment regimen in the future? It sure is looking possible. References: J Neuroinflammation. 2011 Aug...

Air pollution and a common genetic makeup may interact to significantly increase a baby’s risk for autism, USC scientists found. The researchers at USC’s Keck School of Medicine cautioned in an interview that they need to do more studies to replicate their findings. The study, to be published in the January 2014 edition of the journal Epidemiology, found that children with the specific gene who spent their in-utero months and their first year after birth in polluted areas of California had three-fold higher risks for autism disorders. “We need to do more studies, but the genetic disposition and air pollution appear to work together to increase the risk of autism more than the risk of each one alone,” said the study’s lead author, Heather E. Volk, an assistant professor of research in preventive medicine at the medical school. Volk’s earlier work found that children had twice the risk of developing autism if their mothers lived within 1,000 feet of a busy freeway during pregnancy. For this research, Volk collaborated with genetics expert Daniel B. Campbell, an assistant professor in psychiatry and behavioral science at the USC medical school. Campbell explained by telephone that roughly half the population has what geneticists call the “MET receptor tyrosine kinase gene.” The gene is found in about 60 percent of people who have autism, indicating that those with the gene have a higher risk, he said. THE CHILDREN To probe the potential interplay between the gene and air quality, Volk, Campbell and their colleagues analyzed the genetics and air pollution exposures of 408 children in the Sacramento, San Francisco and Los Angeles areas; the children’s cases already were being tracked for research purposes. Of those children, 252 met the diagnostic criteria for the spectrum of autism disorders. Using regional air quality readings and traffic proximity data, the research team determined each child’s air pollution exposure while they were fetuses and in their first year after birth — a critical period in the development of the brain and other organs. The scientists used a blood test to determine each child’s genetics. The team found no increase in the autism risk among the children who had the gene but breathed relatively clean air. But those who had the gene and were exposed to air pollution were three times more likely to have the disease, Volk said. Beth Burt, president of the Autism Society Inland Empire, said she appreciates the research. “It is fascinating and important work,” said Burt, a Corona resident who has an autistic son who is 20. “It is not an either/or situation — genetics or the environment,” she said. “But it may be the combination of a genetic predisposition with an environmental trigger.” Lillian Vasquez, who also has a 20-year-old son with autism, said she was not surprised by USC’s findings. She said she has always thought autism was the result of genetics and some sort of trigger, such as a vaccination or an artificial sweetener. “Air pollution as a trigger seems quite plausible,” she said. Vasquez, vice president of the Inland autism society, has lived in Colton since before her pregnancy. Colton, like most of the Inland area, has long had unhealthful levels of air pollution. OTHER RESEARCH Autism disorders are incurable, lifelong brain disabilities characterized by problems with social interaction,...

Could eating meat from animals infected with one type of Clostridia bacteria be the MS ‘smoking gun?’ Researchers may have unearthed a trigger for multiple sclerosis (MS) that’s been hiding in plain sight. Scientists from Weill Cornell Medical College and Rockefeller University have identified a bacterium they believe can trigger MS—and it’s found just about everywhere, including dirt. Their study, published in PLOS ONE, is the first to identify the bacterium, Clostridium (C.) perfringens type B, in humans. They first identified it in the blood of a 21-year-old woman with MS who was having a relapse. She was part of the Harboring the Initial Trigger for MS (HITMS) observational study launched by Timothy Vartanian, a professor of neurology and neuroscience at Weill Cornell Medical College and director of the Judith Jaffe Multiple Sclerosis Center at New York-Presbyterian Hospital and Weill Cornell, and Kareem Rashid Rumah, an MD/PhD student at Weill Cornell and lead investigator. See 13 Early Signs of MS » Getting the Dirt on C. perfringens C. perfringens, found in soil, is one of the most common types of bacteria in the world. It has five subsets, A through D. Type A commonly occurs in the human gastrointestinal tract and is thought to be harmless. Types B and D, however, can emit a harmful substance called epsilon toxin when eaten by grazing livestock. The substance travels through the bloodstream, crossing the blood-brain barrier and destroying myelin, causing MS-like symptoms in the animals. Vartanian, Rashid, and their team wondered if C. perfringens types B or D could be identified in humans. They tested the blood of both MS patients and healthy control subjects. In samples from MS patients, the levels of antibodies to the toxins were 10 times higher than in the healthy controls. They also noted that only one sample in 100 from the healthy controls showed any sign of exposure to the bacteria. Researchers hypothesize that eating grazing animals who are infected with the bacteria could be the way C. perfringens Type B is introduced into the human digestive system. The human gut plays host to many types of bacteria, not all of them bad. Some are actually necessary for maintaining good health. Researchers suppose that the reason one person reacts to the toxin emitted by the bacteria while another does not may depend on the natural balance of bacteria in a person’s gut. Learn 6 Surprising Facts About the Microbes Living in Your Gut » “We believe the toxin enters the blood from the gut,” said Vartanian in an interview with Healthline. “Once in the blood, the toxin binds to a specific receptor present on the [lining of] the brain blood vessels, resulting in injury to the blood brain barrier (BBB). The toxin in the blood can then enter the brain at focal sites of BBB injury and bind to the same receptor on oligodendrocytes, the myelin forming cells of the central nervous system, resulting in oligodendrocyte death.” Bacterial “Relapses” The type B bacteria, once settled in the gut, goes through growth cycles followed by periods of dormancy. Since the toxin is only emitted during active periods, it is not always present in the bloodstream. Researchers are intrigued by this cyclical activity and hope to investigate whether these growth cycles coincide with relapses in people with relapsing-remitting forms of MS. “We are working on that now and...

It may sound like witchcraft, but Berkeley scientists have found that ticks who feast on the blood of the common western fence lizard are purged of any Lyme disease bacteria hiding in their gut. The newly published findings may explain why there is less tick-borne Lyme disease in California than in the eastern United States, where the debilitating illness was first discovered and given its name. Researchers suspect that a yet- to-be-identified protein in the lizard’s blood destroys the microbes that would otherwise flourish in the tick’s belly and can be later transmitted to human victims. “We’ve speculated on this for years, and now we have fairly good evidence that this is the case,” said Robert Lane, a University of California at Berkeley insect biologist who has been studying ticks and Lyme disease for more than a decade. Lane and his colleague Gary Quistad conducted a series of laboratory experiments using young Lyme disease-infected ticks and fence lizards. In the nymphal stage during which they feed on the blood of lizards, the ticks are only about the size of a poppy seed. But it is common to find 30 to 40 at one time sharing the blood of a single fence lizard. Although infected adult female ticks pose a serious threat of transmitting Lyme disease to humans, the smaller nymphal ticks are the most dangerous because they are harder to find and are still capable of transmitting the disease. Lane had determined eight years ago that the lizards appeared to be immune to Lyme disease despite infestation with tick nymphs. His latest research, published recently in the Journal of Parasitology, suggest why this happens. The experiments first ruled out the possibility that antibodies produced by the lizard’s immune system were able to neutralize the Lyme disease bacteria. Test tube experiments found that Lyme disease bacteria bathed in lizard’s blood died within one hour, while control samples grown in mouse blood lasted three days. In another experiment, the researchers heated lizard blood to the boiling point, and found that it no longer killed the bacteria in a test tube. The sum of these tests points to what Lane calls a “spirochete-killing factor” that is probably a large protein. “It’s an extremely important paper,” said Vicky Kramer, chief of the vector-borne disease section of the California Department of Health Services. Researchers are now trying to determine the precise nature of the Lyme disease-killing protein, and perhaps find out if it can be used to create a treatment for the disease. Lane said he has not yet discussed his findings with biotechnology companies. California health officials long have been pleasantly puzzled by the fact that Lyme disease is a relative rarity in the state, despite an abundance of ticks. Lane points out that in the eastern regions with higher Lyme disease rates, “they don’t have fence lizards there.” Berkeley’s Tilden Park served as the field laboratory for Lane, where he previously also uncovered a curious quirk about Lyme disease and the black-legged ticks that carry it there: the infection rates for young ticks, while low, was three to four times higher than the rate in adult ticks. The latest findings again suggest why: When young nymphal ticks feed on the fence lizards, the mysterious protein not only protects the lizard from infection...

Joint research from the University of Alabama at Birmingham Department of Psychology and Auburn University indicates that brain scans show signs of autism that could eventually support behavior-based diagnosis of autism and effective early intervention therapies. The findings appear online today in Frontiers in Human Neuroscience as part of a special issue on brain connectivity in autism. “This research suggests brain connectivity as a neural signature of autism and may eventually support clinical testing for autism,” said Rajesh Kana, Ph.D., associate professor of psychology and the project’s senior researcher. “We found the information transfer between brain areas, causal influence of one brain area on another, to be weaker in autism.” The investigators found that brain connectivity data from 19 paths in brain scans predicted whether the participants had autism, with an accuracy rate of 95.9 percent. Kana, working with a team including Gopikrishna Deshpande, Ph.D., from Auburn University’s MRI Research Center, studied 15 high-functioning adolescents and adults with autism, as well as 15 typically developing control participants ages 16-34 years. Kana’s team collected all data in his autism lab at UAB that was then analyzed using a novel connectivity method at Auburn. The current study showed that adults with autism spectrum disorders processed social cues differently than typical controls. It also revealed the disrupted brain connectivity that explains their difficulty in understanding social processes. “We can see that there are consistently weaker brain regions due to the disrupted brain connectivity,” Kana said. “There’s a very clear difference.” Participants in this study were asked to choose the most logical of three possible endings as they watched a series of comic strip vignettes while a functional MRI scanner measured brain activity. The scenes included a glass about to fall off a table and a man enjoying the music of a street violinist and giving him a cash tip. Most participants in the autism group had difficulty in finding a logical end to the violinist scenario, which required an understanding of emotional and mental states. The current study showed that adults with autism spectrum disorders struggle to process subtle social cues, and altered brain connectivity may underlie their difficulty in understanding social processes. “We can see that the weaker connectivity hinders the cross-talk among brain regions in autism,” Kana said. Kana plans to continue his research on autism. “Over the next five to 10 years, our research is going in the direction of finding objective ways to supplement the diagnosis of autism with medical testing and testing the effectiveness of intervention in improving brain connectivity,” Kana said. Autism is currently diagnosed through interviews and behavioral observation. Although autism can be diagnosed by 18 months, in reality, earliest diagnoses occur around ages 4-6 as children face challenges in school or social settings. “Parents usually have a longer road before getting a firm diagnosis for their child now,” Kana said. “You lose a lot of intervention time, which is so critical. Brain imaging may not be able to replace the current diagnostic measures; but if it can supplement them at an earlier age, that’s going to be really helpful.” The findings of this study build on Kana’s research collaborations with Auburn that began in 2010. Lauren Libero, a graduate student in the UAB Department of Psychology, assisted in the research. READ...

NEW YORK (GenomeWeb News) – Methylation marks across the human genome may make up an “epigenetic clock” for gauging the chronological age of various tissues in the human body, according to a study published online last night in Genome Biology. A University of California at Los Angeles researcher used a computational method to fish out more than 350 age-informative cytosine methylation markers from thousands of healthy samples collected across the human lifespan and profiled using microarrays for prior studies. Findings from the study suggest the resulting methylation-based aging predictor can accurately determine chronological age across multiple tissue types. The work also offered insights into how tissues age with time and revealed differences in aging profiles between tissues and in tumor samples. More work is needed to untangle the nature of the relationship between age and the methylation profiles described in the study. “The big question is whether the biological clock controls a process that leads to aging,” the study’s author, Steve Horvath, a human genetics and biostatistics researcher affiliated with UCLA’s David Geffen School of Medicine and the UCLA Fielding School of Public Health, said in a statement. “If so, the clock will become an important biomarker for studying new therapeutic approaches to keeping us young,” he added. In an effort to explore previously proposed ties between aging and epigenetics, Horvath brought together cytosine methylation profiles that had been ascertained for 7,844 samples using Illumina 27K or 450K arrays. The sample represented 51 non-cancerous human tissue and/or cell types and came from 82 different datasets, Horvath noted. With a training set that included 39 of the datasets, he used a so-called elastic net regression model to whittle down to a set of 352 cytosine methylation marks that appeared promising for predicting the age of multiple tissues. This methylation-based epigenetic clock was subsequently validated in healthy samples from dozens more studies before being used to assess aging patterns at specific cell stages or in tissue types. After establishing these methylation-based clocks in normal tissues, for instance, Horvath turned his attention to 5,826 cancer samples from 32 different DNA methylation datasets. That arm of the analysis indicated that the ability to predict age using the methylation clock tends to break down somewhat in tumor samples. Generally speaking, though, cancers have DNA methylation “ages” beyond their years and appear far older than corresponding non-cancerous tissue. That was especially true for tumors containing relatively modest somatic mutation burdens. It was also the case for some of the breast cancer samples examined in the study, though even normal breast tissue appeared to acquire more aged methylation marks than other tissues of the same chronological age. “Healthy breast tissue is about two to three years older than the rest of a woman’s body,” Horvath noted. “If a woman has breast cancer, the healthy tissue next to the tumor is an average of 12 years older than the rest of her body.” Breast tissue was one of the tissue types that showed less precise calibration on the DNA methylation-based aging clock, Horvath noted, particularly in the cancerous cases. But for samples from women without cancer, the epigenetic clock came up with age estimates that were within around seven-and-a-half years of individuals’ chronological age, on average. Induced pluripotent stem cells had “young” or “reset” epigenetic clocks, according...